TBE 31

TBE-31 (0.03-0.3 μM; topical administration; once every 24 hours; 3 consecutive doses) dose-dependently increases skin NQO1 activity up to 4.9-fold and GST activity up to 1.5-fold in healthy SKH-1 hairless mice^[1].
TBE-31 (administered orally at 0.1-0.3 μM per 3 g of feed, once daily for 11 days) dose-dependently increases the activity and protein levels of cytoprotective enzymes by up to 5.0-fold in the liver, skin and stomach (but not the cerebral cortex) of healthy SKH-1 hairless mice, with no observed toxicity^[1].
A single oral administration of TBE-31 (10 μM/kg) increases NQO1 activity by 2.4-fold in the liver and 1.5-fold in the heart of female C57BL/6 mice^[2].
TBE-31 (40 nM per animal; topical administration; twice weekly; for approximately 30 weeks) significantly reduces the tumor number and burden in a UV-induced skin carcinogenesis mouse model with concurrent immunosuppression by Azathioprine (HY-B0256)^[2].
TBE-31 (1-10 mg/kg; p.o.; single administration) exerts a dose-dependent anti-inflammatory effect on LPS (HY-D1056)-induced elevation of TNF-α, and significantly ameliorates LPS-induced depressive-like behaviors in mice at the dose of 10 mg/kg^[3].
Treatment with TBE-31 (5 nM/g; p.o.; three times per week for 6 weeks) reverses diet-induced insulin resistance, alleviates hepatic steatosis, and improves non-alcoholic steatohepatitis (NASH) and liver fibrosis in diseased Nrf2^+/+ mice; NAS is reduced by 40.8%, while glucose homeostasis, oxidative stress and inflammatory markers are all improved^[4].
TBE-31 (5 nM/g; p.o.; three times per week; for 6 weeks) requires functional Nrf2 to improve insulin sensitivity, reduce hepatic steatosis, and alleviate non-alcoholic steatohepatitis (NASH) in mice with established diet-induced disease. These beneficial effects are completely abolished in Nrf2^-/- mice, whereas the NAS is reduced by 52.9% in Nrf2^+/+ mice^[4].